title: Cerebral amyloid angiopathy pathology and cognitive domains in older persons.
abstract: OBJECTIVE
  To examine the relation of cerebral amyloid angiopathy (CAA) to cognitive domains in older community-dwelling persons with and without dementia.
  
  
  METHODS
  Subjects were 404 persons in the Religious Orders Study, a cohort study of aging, who underwent annual clinical evaluations, including 19 neuropsychological tests from which 5 cognitive domain and global summary scores were derived, and brain autopsy at time-of-death (mean age-at-death 86). Using amyloid-β immunostaining, CAA severity was graded in 5 regions (midfrontal, inferior temporal, angular, calcarine, and hippocampal cortices), as 0 = none, 1 = mild, 2 = moderate, 3 = severe, and 4 = very severe. Because severity was related across regions (all r(s) > 0.63), and almost all persons had some CAA, we averaged regional CAA scores and created class variable predictors for no-to-minimal (<0.5), mild-to-moderate (0.5-2.5) and moderate-to-very severe CAA (>2.5).
  
  
  RESULTS
  CAA was very common (84.9%; 94 had no-to-minimal, 233 mild-to-moderate, and 76 moderate-to-very severe disease) and was related to AD pathology (r(s) = 0.68). In linear regression analyses controlling for age, sex, education, AD pathology, infarcts, and Lewy bodies, moderate-to-very severe CAA was associated with lower perceptual speed (p = 0.012) and episodic memory (p = 0.047), but not semantic memory, working memory, visuospatial skills, or a composite of all cognitive measures. No associations of mild-to-moderate CAA with cognition were found. Dementia did not modify these findings.
  
  
  CONCLUSIONS
  CAA pathology is very common in older community-dwelling persons and is associated with AD pathology. Moderate-to-very severe CAA, but not mild-to-moderate CAA, is associated with lower performance in specific cognitive domains, most notably perceptual speed, separately from the effect of AD pathology.
authors.affiliation: Rush Alzheimer's Disease Center, Chicago, IL, USA.
authors.forename: Zoe
authors.initials: Z
authors.lastname: Arvanitakis
authors.forename: Sue E
authors.initials: SE
authors.lastname: Leurgans
authors.forename: Zhenxin
authors.initials: Z
authors.lastname: Wang
authors.forename: Robert S
authors.initials: RS
authors.lastname: Wilson
authors.forename: David A
authors.initials: DA
authors.lastname: Bennett
authors.forename: Julie A
authors.initials: JA
authors.lastname: Schneider
mesh_terms: D000375:Aging / Q000473:pathology*; D000682:Amyloid / Q000378:metabolism; D001921:Brain / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D016657:Cerebral Amyloid Angiopathy / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D003071:Cognition / Q000502:physiology*; D003072:Cognition Disorders / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D003704:Dementia / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D016014:Linear Models; D008137:Longitudinal Studies; D009483:Neuropsychological Tests; D012720:Severity of Illness Index
chemical_list: D000682:Amyloid